Vasomotor Control of the Liver Circulation

Abstract

Our present knowledge of the vasomotor control of the liver circulation is curiously inadequate. In due time the evidence for this conclusion will be reviewed in detail; now we wish merely to record a summary of the results which have been obtained during the last couple of years in a study of this problem, using cats under chloralose anesthesia and the liver plethysmograph previously referred to. 1 , 2

The peripheral vagus has no effect on liver volume; we have stimulated it in the neck (after denervating the heart according to Cannon's method), below the heart in the thorax and after emerging through the diaphragm.

The postganglionic fibers of the hepatic plexus constrict not only the terminals of the hepatic artery but also those of the portal vein.

The preganglionic fibers of the splanchnic (left) have exactly the same effect on liver volume, either by way of the artery or portal vein, as stimulation of the postganglionic fibers in the hepatic plexus.

Reflex pressor responses are accompanied by decreased liver volume; depressor reflexes produce dilation in the liver. If, however, the liver is denervated by cutting the fibers of the hepatic plexus, its volume then follows passively the general blood pressure.

During the generalized vasomotor activity induced by asphyxia (rebreathing the air in a small balloon) the liver constricts powerfully during the rise of general blood pressure and remains constricted even as the heart begins to fail. If it is denervated, however, it dilates for a time as the general blood pressure is rising; but before this has reached its maximum the liver often begins to constrict maximally. This delayed constriction may be prevented by removal of the adrenals; then the denervated liver volume passively follows the general blood pressure throughout the course of the asphyxia.